Research Paper Volume 13, Issue 7 pp 9820—9837

Inhibition of HDAC6 by Tubastatin A reduces chondrocyte oxidative stress in chondrocytes and ameliorates mouse osteoarthritis by activating autophagy

HDAC6 selective inhibitor TubA prevents TBHP-induced apoptosis in chondrocytes. (A) The cell viability of chondrocytes at 24 hours after different concentrations of TubA treatment. (B) The cell viability of chondrocytes treated with TubA at a concentration of 100 μM in a time-dependent manner. (C) The cell viability of chondrocytes at 24 hours after co-treatment of TBHP and TubA for 6 hours. (D–F) Western blotting and quantification of HDAC6 and acetyl-α-tubulin in each group. Chondrocytes were treated TBHP or/and TubA for 6 hours. (G–J) Western blotting and quantification of apoptotic markers in each chondrocyte group as above. (K, L) IF staining and quantification of cleaved caspase 3 in each chondrocyte group as above, scale bar = 100 μm, scale bar (enlarged) = 20 μm. N = 5, GAPDH was the loading control, significance: *P

Figure 2. HDAC6 selective inhibitor TubA prevents TBHP-induced apoptosis in chondrocytes. (A) The cell viability of chondrocytes at 24 hours after different concentrations of TubA treatment. (B) The cell viability of chondrocytes treated with TubA at a concentration of 100 μM in a time-dependent manner. (C) The cell viability of chondrocytes at 24 hours after co-treatment of TBHP and TubA for 6 hours. (DF) Western blotting and quantification of HDAC6 and acetyl-α-tubulin in each group. Chondrocytes were treated TBHP or/and TubA for 6 hours. (GJ) Western blotting and quantification of apoptotic markers in each chondrocyte group as above. (K, L) IF staining and quantification of cleaved caspase 3 in each chondrocyte group as above, scale bar = 100 μm, scale bar (enlarged) = 20 μm. N = 5, GAPDH was the loading control, significance: *P<0.05, **P<0.01, ***P<0.001.